Detection and identification of Bogia coconut syndrome phytoplasma from seed-associated tissues and seedlings of coconut (Cocos nucifera) and betel nut (Areca catechu).

Evidence for seed transmission of phytoplasmas has grown in several pathosystems including coconut (Cocos nucifera). Bogia coconut syndrome (BCS) is a disease associated with the lethal yellowing syndrome associated with the presence of 'Candidatus Phytoplasma noviguineense' that affects coconut, betel nut (Areca catechu) and bananas (Musa spp.) in Papua New Guinea. Coconut and betel nut drupes were sampled from BCS-infected areas in Papua New Guinea, dissected, the extracted nucleic acid was used in polymerase chain reaction (PCR), and loop mediated isothermal amplification (LAMP) used to check for presence of phytoplasma DNA. In a second study, drupes of both plant species were collected from multiple field sites and grown in insect-proof cages. Leaf samples taken at 6 months were also tested with PCR and LAMP. The studies of dissected coconut drupes detected phytoplasma DNA in several tissues including the embryo. Drupes from betel nut tested negative. Among the seedlings, evidence of possible seed transmission was found in both plant species. The results demonstrate the presence of 'Ca. P. noviguineense' in coconut drupes and seedlings, and in seedlings of betel nut; factors that need to be considered in ongoing management and containment efforts.

Utilizing Cationic Vacancies and Spontaneous Polarization on Cathode to Enhance Zinc-Ion Storage and Inhibit Dendrite Growth in Zinc-Ion Batteries.

High energy density and intrinsic safety are the central pursuits in developing rechargeable Zinc-ion batteries (ZIBs). The capacity and stability of nickel cobalt oxide (NCO) cathode are unsatisfactory because of its semiconductor character. Herein, we propose a built-in electric field (BEF) approach by synergizing cationic vacancies and ferroelectric spontaneous polarization on cathode side to facilitate electron adsorption and suppress zinc dendrite growth on the anode side. Concretely, NCO with cationic vacancies was constructed to expand lattice spacing for enhanced zinc-ion storage. Heterojunction with BEF leads to the Heterojunction//Zn cell exhibiting a capacity of 170.3 mAh g-1 at 400 mA g-1 and delivering a competitive capacity retention of 83.3 % over 3000 cycles at 2 A g-1 . We conclude the role of spontaneous polarization in suppressing zinc dendrite growth dynamics, which is conducive to developing high-capacity and high-safety batteries via tailoring defective materials with ferroelectric polarization on the cathode.

Oxygen-enriched lignin-derived porous carbon nanosheets promote Zn2+ storage.

Carbon-based zinc-ion capacitors (ZICs) have sparked intense research enthusiasm because of large power density, good rate capability and cycling stability. However, there is still a long way to go before they achieve commercial applications. Herein, oxygen-enriched lignin-derived porous carbon nanosheets (OLCKs) were prepared by one-step carbonization-activation method, and more O-containing functional groups were generated on the surface of the porous carbon by post-surface functionalization strategy. The self-doped N can change the electron distribution of carbon skeleton and decrease energy barrier of chemical absorption of Zn2+/H+. Meanwhile, the carbonyl group can significantly enhance the wettability of OLCKs. Furthermore, the diffusion-controlled reactions mainly exist at high and low potential ranges in CV curves, which demonstrates the occurred Faradaic reaction. Consequently, the assembled aqueous ZICs based on OLCKs demonstrate a capacity of 121.7 mAh/g at 0.3 A/g, energy density of 94.3 Wh kg-1 and good cyclic stability. Besides, the assembled Zn//PVA/LiCl/ZnCl2(gel)//OLCK4 ZIC can also achieve energy density of 134.4 Wh kg-1 at 0.1 A/g. This work provides a novel design strategy by incorporating abundant O and N-containing functional groups to enhance energy density.

Enhanced adsorption and photocatalytic Cr(VI) reduction and sterilization of defective MoS2/PVP.

The exploration of novel nanomaterials to resolve the issues of water pollution with the aid of photocatalytic technology has always been a research hotspot. MoS2 is acknowledged to be one of the promising photocatalysts for its interesting layered structure, suitable band gap, and good chemical stability. However, the fast recombination of photogenerated electrons and holes within the MoS2 impedes its extensive application. Here, hydrophilic polymer (polyvinyl pyrrolidone, PVP) and sulfur vacancy (Vs) are simultaneously introduced into the MoS2 nanosheets to achieve high-efficient photocatalytic hexavalent chromium Cr(VI) removal and antibacterial performance. The incorporation of PVP greatly enhances the adsorption capacity of MoS2, and creating Vs essentially strengthens the photogenerated carrier separation of MoS2. As a result, the Cr(VI) removal efficiency of MoS2-PVP with an appropriate Vs concentration is up to 99.5 % for 3 h. Meanwhile, MoS2-PVP with a relatively higher Vs concentration displays a superior Escherichia coli (E. coli) removal efficiency of 91.8 % within 30 min with the initial E. coli concentration of âˆ¼1.0 × 107 CFU/mL. This study extends photocatalysts to a higher level in designing advanced materials for environmental remediation and establishes a feasible platform for emphasizing the versatility of defect engineering in regulating catalytic activity.

Oxygen-Deficient α-MnO2 Nanotube/Graphene/N, P Codoped Porous Carbon Composite Cathode To Achieve High-Performing Zinc-Ion Batteries.

A major drawback of α-MnO2-based zinc-ion batteries (ZIBs) is the poor rate performance and short cycle life. Herein, an oxygen-deficient α-MnO2 nanotube (VO-α-MnO2)-integrated graphene (G) and N, P codoped cross-linked porous carbon nanosheet (CNPK) composite (VO-α-MnO2/CNPK/G) has been prepared for advanced ZIBs. The introduction of VO in MnO2 can decrease the value of the Gibbs free energy of Zn2+ adsorption near VO (ca. -0.73 eV) to the thermal neutral value. The thermal neutral value demonstrates that the Zn2+ adsorption/desorption process on VO-α-MnO2 is more reversible than that on α-MnO2. The as-made Zn/VO-α-MnO2 battery is able to deliver a large capacity of 305.0 mAh g-1 and high energy density up to 408.5 Wh kg-1. The good energy storage properties can be attributed to VO. Additionally, the VO-α-MnO2/CNPK/G composite possesses the structure of nanotube arrays, which results from the vertical growth of α-MnO2 nanotubes on CNPK. This unique array structure helps to realize fast ion/electron transfer and stable microstructure. The electrochemical performance of VO-α-MnO2 has been comprehensively improved by compositing with G and CNPK. The VO-α-MnO2/CNPK/G can achieve capacity up to 405.2 mAh g-1, energy density of 542.2 Wh kg-1, and long cycle life (80% capacity retention after 2000 cycles).

Effectiveness of collateral arteries embolization before endovascular aneurysm repair to prevent type II endoleaks: A systematic review and meta-analysis.

OBJECTIVES: This study aimed to evaluate the effect of preventive collateral arteries embolization before endovascular aneurysm repair (EVAR) to reduce type II endoleaks (T2EL), aneurysm enlargement, and re-interventions. METHODS: A comprehensive search of PubMed, MEDLINE, Web of Science, and Embase was conducted to identify articles in English, related to preventive collateral arteries embolization before EVAR, published until October 2020. RESULTS: A total of 12 relevant studies, including 11 retrospective studies and one randomized controlled trial, were identified and fulfilled the specified inclusion criteria. A total of 1706 patients in 11 studies were involved in the meta-analysis. The overall incidence of T2EL was 17.3% in the embolization group vs. 34.5% in the control group (OR 0.36, p < 0.01). The incidence of persistent T2EL was 15.3% vs. 30.0% (OR 0.37, p < 0.01). Five studies reported the incidence of sac enlargement, with the rate 10.2% vs. 24.9% (OR 0.25, p < 0.01). Nine studies reported T2EL related re-interventions, and it was 1.3% in the embolization group and 10.4% in control (OR 0.14, p < 0.01). The technical success of collateral arteries embolization was 92.1% (455/494) in the 12 studies. 1.2% (10/829) patients suffered a mild complication of collateral arteries embolization, and 2/829 patients died because of the embolization. CONCLUSION: Collateral arteries embolization is a promising measure to prevent the occurrence of T2EL, sac enlargement, and re-intervention. High-quality studies need to be conducted to provide stronger evidence-based medical suggestions about the embolize operation.

The Efficacy of Transcarotid Artery Revascularization With Flow Reversal System Compared to Carotid Endarterectomy: A Systematic Review and Meta-Analysis.

Background: Carotid artery stenosis has long been a critical cause of stroke and death, and it can seriously affect the life quality. Transcarotid artery revascularization (TCAR) and carotid endarterectomy (CEA) are both feasible therapies for this disease. This systematic review and meta-analysis aim to evaluate if the efficacy of the two approaches is comparable. Methods: Clinical studies up to March 2021 were searched through PubMed, Embase, and Scopus from a computer. The screening process was designed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement. Newcastle-Ottawa Scale (NOS) was used for methodological quality assessment of works of literature meeting the inclusion criteria, and Review Manager 5.4 was used for data synthesis. The I2 statistic was performed to measure the heterogeneity, and M-H/I-V fixed or random model was utilized depending on the I2 value. The evidence evaluation was accomplished based on grades of recommendation, assessment, development, and evaluation (GRADE) online tool. Results: A total of 14,200 subjects (six comparative studies) were finally included in this pooled study. There is no statistical discrepancy between the two treatments on reducing stroke/death/myocardial infarction (odds ratio [OR] 0.85, 95% CI 0.67-1.07), stroke (OR 1.03, 95% CI 0.77-1.37), or death (OR 1.14, 95% CI 0.67-1.94). Besides, TCAR is associated with a lower incidence of myocardial infarction (P = 0.004), cranial nerve injury (P < 0.00001), and shorter procedure time (P < 0.00001) than CEA among the overall cohort. Conclusions: TCAR is a rapidly developing treatment that reaches a comparable prognosis to CEA and significantly reduces the risk of myocardial infarction under the well-matched condition, which is a dependable choice for patients with carotid stenosis.

Evolution of Superconducting Properties in Fe1.1Se0.8Te0.2 Films Before and After Structure Avalanche.

By preparing a series of high-quality Fe1.1Se0.8Te0.2 films on the CaF2 substrate via pulsed laser deposition, we reveal the evolution of the structure as well as the superconductivity with the film thickness. We have found that there exists a threshold thickness above which the critical temperature Tc reaches its optimal value of 23.18 K with large activation energy, promising for high-field technological applications. Most importantly, the thick films have been found in a metastable state due to the fragile balance between the increased strain energy and the large compressive stress. Once the balance is broken by an external perturbation, a unique structure avalanche happens with a large part of the film exfoliated from the substrate and curves out. The exfoliated part of the film remains a single phase, with its lattice parameter and Tc recovering the bulk values. Our results clearly demonstrate the close relation between the compressive stress of the film/substrate interface and the high critical temperature observed in FeSeTe films. Moreover, this also provides an efficient way to fabricate free-standing single-phase FeSeTe crystals in the phase-separation regime.

Nf1 heterozygous mice recapitulate the anthropometric and metabolic features of human neurofibromatosis type 1.

Neurofibromatosis type 1 (NF1) is a heritable cancer predisposition syndrome resulting from mutations in the NF1 tumor suppressor gene. Genotype-phenotype correlations for NF1 are rare due to the large number of NF1 mutations and role of modifier genes in manifestations of NF1; however, emerging reports suggest that persons with NF1 display a distinct anthropometric and metabolic phenotype featuring short stature, low body mass index, increased insulin sensitivity, and protection from diabetes. Nf1 heterozygous (Nf1+/-) mice accurately reflect the dominant inheritance of NF1 and are regularly employed as a model of NF1. Here, we sought to identify whether Nf1+/- mice recapitulate the anthropometric and metabolic features identified in persons with NF1. Littermate 16-20 week-old male wildtype (WT) and Nf1+/- C57B/6J mice underwent nuclear magnetic resonance (NMR), indirect calorimetry, and glucose/insulin/pyruvate tolerance testing. In some experiments, tissues were harvested for NMR and histologic characterization. Nf1+/- mice are leaner with significantly reduced visceral and subcutaneous fat mass, which corresponds with an increased density of small adipocytes and reduced leptin levels. Additionally, Nf1+/- mice are highly reliant on carbohydrates as an energy substrate and display increased glucose clearance and insulin sensitivity, but normal response to pyruvate suggesting enhanced glucose utilization and preserved gluconeogenesis. Finally, WT and Nf1+/- mice subjected to high glucose diet were protected from diet-induced obesity and hyperglycemia. Our data suggest that Nf1+/- mice closely recapitulate the anthropometric and metabolic phenotype identified in persons with NF1, which will impact the interpretation of previous and future translational studies of NF1.

Mechanism and consequences for avoidance of superparasitism in the solitary parasitoid Cotesia vestalis.

A parasitoid's decision to reject or accept a potential host is fundamental to its fitness. Superparasitism, in which more than one egg of a given parasitoid species can deposit in a single host, is usually considered sub-optimal in systems where the host is able to support the development of only a single parasitoid. It follows that selection pressure may drive the capacity for parasitoids to recognize parasitized hosts, especially if there is a fitness cost of superparasitism. Here, we used microsatellite studies of two distinct populations of Cotesia vestalis to demonstrate that an egg laid into a diamondback moth (Plutella xylostella) larva that was parasitized by a conspecific parasitoid 10 min, 2 or 6 h previously was as likely to develop and emerge successfully as was the first-laid egg. Consistent with this, a naive parasitoid encountering its first host was equally likely to accept a healthy larva as one parasitized 10 min prior, though handling time of parasitized hosts was extended. For second and third host encounters, parasitized hosts were less readily accepted than healthy larvae. If 12 h elapsed between parasitism events, the second-laid egg was much less likely to develop. Discrimination between parasitized and healthy hosts was evident when females were allowed physical contact with hosts, and healthy hosts were rendered less acceptable by manual injection of parasitoid venom into their hemolymph. Collectively, these results show a limited capacity to discriminate parasitized from healthy larvae despite a viability cost associated with failing to avoid superparasitism.

3D N,O-Codoped Egg-Box-Like Carbons with Tuned Channels for High Areal Capacitance Supercapacitors.

Functional carbonaceous materials for supercapacitors (SCs) without using acid for post-treatment remain a substantial challenge. In this paper, we present a less harmful strategy for preparing three-dimensional (3D) N,O-codoped egg-box-like carbons (EBCs). The as-prepared EBCs with opened pores provide plentiful channels for ion fast transport, ensure the effective contact of EBCs electrodes and electrolytes, and enhance the electron conduction. The nitrogen and oxygen atoms doped in EBCs improve the surface wettability of EBC electrodes and provide the pseudocapacitance. Consequently, the EBCs display a prominent areal capacitance of 39.8 µF cm-2 (340 F g-1) at 0.106 mA cm-2 in 6 M KOH electrolyte. The EBC-based symmetric SC manifests a high areal capacitance to 27.6 µF cm-2 (236 F g-1) at 0.1075 mA cm-2, a good rate capability of 18.8 µF cm-2 (160 F g-1) at 215 mA cm-2 and a long-term cycle stability with only 1.9% decay after 50,000 cycles in aqueous electrolyte. Impressively, even in all-solid-state SC, EBC electrode shows a high areal capacitance of 25.0 µF cm-2 (214 F g-1) and energy density of 0.0233 mWh cm-2. This work provides an acid-free process to prepare electrode materials from industrial by-products for advanced energy storage devices.

Loss of GTPase activating protein neurofibromin stimulates paracrine cell communication via macropinocytosis.

Neurofibromin, the protein product of the neurofibromatosis type 1 (NF1) tumor suppressor gene, is a negative regulator of Ras signaling. Patients with mutations in NF1 have a strong predisposition for cardiovascular disease, which contributes to their early mortality. Nf1 heterozygous (Nf1+/-) bone marrow to wild type chimeras and mice with heterozygous recombination of Nf1 in myeloid cells recapitulate many of the vascular phenotypes observed in Nf1+/- mutants. Although these results suggest that macrophages play a central role in NF1 vasculopathy, the underlying mechanisms are currently unknown. In the present study, we employed macrophages isolated from either Nf1+/- or Lysm Cre+/Nf1f/f mice to test the hypothesis that loss of Nf1 stimulates macropinocytosis in macrophages. Scanning electron microscopy and flow cytometry analysis of FITC-dextran internalization demonstrated that loss of Nf1 in macrophages stimulates macropinocytosis. We next utilized various cellular and molecular approaches, pharmacological inhibitors and genetically modified mice to identify the signaling mechanisms mediating macropinocytosis in Nf1-deficient macrophages. Our results indicate that loss of Nf1 stimulates PKCδ-mediated p47phox phosphorylation via RAS activation, leading to increased NADPH oxidase 2 activity, reactive oxygen species generation, membrane ruffling and macropinocytosis. Interestingly, we also found that Nf1-deficient macrophages internalize exosomes derived from angiotensin II-treated endothelial cells via macropinocytosis in vitro and in the peritoneal cavity in vivo. As a result of exosome internalization, Nf1-deficient macrophages polarized toward an inflammatory M1 phenotype and secreted increased levels of proinflammatory cytokines compared to controls. In conclusion, the findings of the present study demonstrate that loss of Nf1 stimulates paracrine endothelial to myeloid cell communication via macropinocytosis, leading to proinflammatory changes in recipient macrophages.

Neurofibromin Deficiency Induces Endothelial Cell Proliferation and Retinal Neovascularization.

Purpose: Neurofibromatosis type 1 (NF1) is the result of inherited mutations in the NF1 tumor suppressor gene, which encodes the protein neurofibromin. Eye manifestations are common in NF1 with recent reports describing a vascular dysplasia in the retina and choroid. Common features of NF1 retinopathy include tortuous and dilated feeder vessels that terminate in capillary tufts, increased endothelial permeability, and neovascularization. Given the retinal vascular phenotype observed in persons with NF1, we hypothesize that preserving neurofibromin may be a novel strategy to control pathologic retinal neovascularization. Methods: Nf1 expression in human endothelial cells (EC) was reduced using small hairpin (sh) RNA and EC proliferation, migration, and capacity to form vessel-like networks were assessed in response to VEGF and hypoxia. Wild-type (WT), Nf1 heterozygous (Nf1+/-), and Nf1flox/+;Tie2cre pups were subjected to hyperoxia/hypoxia using the oxygen-induced retinopathy model. Retinas were analyzed quantitatively for extent of retinal vessel dropout, neovascularization, and capillary branching. Results: Neurofibromin expression was suppressed in response to VEGF, which corresponded with activation of Mek-Erk and PI3-K-Akt signaling. Neurofibromin-deficient EC exhibited enhanced proliferation and network formation in response to VEGF and hypoxia via an Akt-dependent mechanism. In response to hyperoxia/hypoxia, Nf1+/- retinas exhibited increased vessel dropout and neovascularization when compared with WT retinas. Neovascularization was similar between Nf1+/- and Nf1flox/+;Tie2cre retinas, but capillary drop out in Nf1flox/+;Tie2cre retinas was significantly reduced when compared with Nf1+/- retinas. Conclusions: These data suggest that neurofibromin expression is essential for controlling endothelial cell proliferation and retinal neovascularization and therapies targeting neurofibromin-deficient EC may be beneficial.

Neurofibromin is a novel regulator of Ras-induced reactive oxygen species production in mice and humans.

Neurofibromatosis type 1 (NF1) predisposes individuals to early and debilitating cardiovascular disease. Loss of function mutations in the NF1 tumor suppressor gene, which encodes the protein neurofibromin, leads to accelerated p21(Ras) activity and phosphorylation of multiple downstream kinases, including Erk and Akt. Nf1 heterozygous (Nf1(+/-)) mice develop a robust neointima that mimics human disease. Monocytes/macrophages play a central role in NF1 arterial stenosis as Nf1 mutations in myeloid cells alone are sufficient to reproduce the enhanced neointima observed in Nf1(+/-) mice. Though the molecular mechanisms underlying NF1 arterial stenosis remain elusive, macrophages are important producers of reactive oxygen species (ROS) and Ras activity directly regulates ROS production. Here, we use compound mutant and lineage-restricted mice to demonstrate that Nf1(+/-) macrophages produce excessive ROS, which enhance Nf1(+/-) smooth muscle cell proliferation in vitro and in vivo. Further, use of a specific NADPH oxidase-2 inhibitor to limit ROS production prevents neointima formation in Nf1(+/-) mice. Finally, mononuclear cells from asymptomatic NF1 patients have increased oxidative DNA damage, an indicator of chronic exposure to oxidative stress. These data provide genetic and pharmacologic evidence that excessive exposure to oxidant species underlie NF1 arterial stenosis and provide a platform for designing novels therapies and interventions.

Combination of Taxol® and dichloroacetate results in synergistically inhibitory effects on Taxol-resistant oral cancer cells under hypoxia.

Cancer cells preferentially catalyze glucose through the glycolytic pathway in the presence of adequate oxygen. This phenomenon is known as the Warburg effect. As is the case with numerous cancer therapeutic agents, resistance remains a significant problem when using Taxol® to treat malignancies. The present study reported that expression of pyruvate dehydrogenase kinase 1 (PDK1) was induced by Taxol treatment at low toxic concentrations in oral cancer cells. In addition, Taxol­resistant cells exhibited upregulated PDK1 protein and mRNA expression. Elevated PDK1 levels contribute to Taxol resistance under hypoxic conditions. Inhibition of PDK1 expression was observed when oral cancer cells were treated with the PDK1 inhibitor dichloroacetate (DCA). The combination of Taxol with DCA showed synergistic inhibitory effects on Taxol­resistant cells under hypoxic conditions; these effects were not observed in Taxol­sensitive oral cancer cells under normoxic conditions. The present study provides a novel mechanism for overcoming Taxol resistance in oral cancer cells, and will contribute towards the development of clinical therapeutics for cancer patients.

Calcium/calmodulin-dependent phosphorylation of tumor protein D52 on serine residue 136 may be mediated by CAMK2delta6.

Tumor protein D52 is expressed at relatively high levels in cells within the gastrointestinal tract that undergo classical exocytosis and is overexpressed in several cancers. Current evidence supports a role for D52 in the regulation of vesicular trafficking. D52 function(s) are regulated by calcium-dependent phosphorylation; however, the intracellular mechanisms that mediate this process are not well characterized. The goal of this study was to identify the calcium-dependent phosphorylation site(s) in D52 and to characterize the protein kinase(s) that mediate this phosphorylation. Using mass spectrometry and site-directed mutagenesis, we identified a single amino acid residue, S(136), that undergoes increased phosphorylation upon elevation of intracellular Ca(2+) concentration. A phosphospecific antibody (pS(136)) was produced and used to characterize D52 kinase activity in gastric mucosal, colonic T84, and HEK293 cells. By using D52 as a substrate, a protein kinase with a molecular weight (M(r)) of approximately 50 kDa was identified with "in gel" assays. This kinase comigrated with rat brain calcium/calmodulin-dependent protein kinase (CAMK2)alpha cross-reacted with pan-specific CAMK2 antibodies as well as with anti-active CAMK2 (pT(286/287)) antibody when activated. Carbachol-stimulated phosphorylation of S(136) was inhibited by the CAMK2 inhibitor KN93 (IC(50) 38 microM) and by the calmodulin antagonist W7 (IC(50) 3.3 nM). A previously uncharacterized CAMK2 isoform, CAMK2delta6, which has the same domain structure and M(r) as CAM2alpha, was identified in gastric mucosa by RT-PCR. The cloned, expressed protein comigrated with D52 kinase and colocalized with D52 protein in T84 and HEK293 cells. These findings support a role for CAMK2delta6 in the mediation of D52 phosphorylation.

Molecular mechanisms of iNOS induction by IL-1 beta and IFN-gamma in rat aortic smooth muscle cells.

In rat aortic smooth muscle cells (RASMC), interferon (IFN)-gamma enhanced nitrite accumulation and type II nitric oxide synthase (iNOS) protein expression induced by interleukin (IL)-1 beta. IFN-gamma alone had no effect on nitrite accumulation or iNOS protein. IL-1 beta, but not IFN-gamma, induced nuclear factor (NF)-kappa B and CCAAT box/enhancer binding protein (C/EBP) nuclear binding. Conversely, IFN-gamma, but not IL-1 beta, induced signal transducer and activator of transcription (STAT) 1 and interferon regulatory factor (IRF)-1 binding. In a -1.4-kb rat iNOS promoter segment, deletion of an IFN-gamma-activated site (GAS) increased IL-1 beta-induced activity but inhibited IFN-gamma-enhanced activity, suggesting a two-way effect of the GAS site on iNOS induction: enhancing induction through STAT1 activation and inhibiting induction through a non-IFN-gamma-mediated mechanism. Deletion of both an IRF and a C/EBP site reduced the IL-1 beta-induced and the IFN-gamma-enhanced activities. However, IRF site mutations decreased the IFN-gamma-enhanced activity without affecting the IL-1 beta-induced activity. Insertion of two IRF sites increased the IFN-gamma-enhanced, but not the IL-1 beta-induced, activity. Mutations of a reverse NF-kappa B site did not significantly change IFN-gamma-enhanced activity. We conclude that in RASMC, NF-kappa B and C/EBP mediate the IL-1 beta-induced iNOS expression, whereas IRF-1 and STAT1 mediate the IFN-gamma-enhanced iNOS induction.