Overexpression of the mango MiCO gene delayed flowering time in transgenic Arabidopsis

Plant Cell, Tissue and Organ Culture (PCTOC) - CONSTANS (CO)/CONSTANS-like (COL) genes play an important role in the photoperiodic flowering pathway. However, the functional roles of the CO/COL...     

Could the recycled yarns substitute for the virgin cotton yarns: a comparative LCA

Purpose

Cotton yarns spun from natural fibers are widely used in the apparel industry. Most of waste cotton goods are now disposed by incineration or landfill, which brings resource and environmental challenges to the society. Using the waste cotton to spin yarns is an alternative way to forward a more sustainable future. In this research, two scenarios for the environmental impacts of yarns spun from corresponding fibers are investigated, including recycled cotton fibers and virgin cotton fibers.

Methods

The life cycle assessment (LCA) has been conducted according to the collected data from on-site investigation of typical production factories. The life cycle for the recycled cotton yarn production is divided into five stages, i.e., raw material acquisition, transportation, breaking, mixing, and spinning. The life cycle of virgin cotton yarn production is been divided into four stages, i.e., raw material acquisition, transportation, mixing, and spinning. The functional unit is 1000 kg produced yarns which are used for weaving into the fabrics. Notable impacts on climate change, fossil depletion, water depletion, and human toxicity were observed.

Results

The life cycle impact assessment (LCIA) results show that environmental impacts of recycled cotton yarns are far less than those of virgin cotton yarns, except for climate change and water depletion. The reason is that the land occupation and irrigation water have great impact on environmental impacts of cotton cultivation. In spinning, the electricity is the key factor whose environmental impacts account for the most in the virgin cotton yarn scenario, while the electricity and water consumptions are the key factors for the recycled cotton yarn scenario in the life cycle of yarn production. The sensitivity analysis indicates that improving energy efficiency can significantly reduce environmental burdens for both the two scenarios. The uncertainty distribution of water depletion, human toxicity, fossil depletion, and climate change of the two scenarios were determined with a 90% confidence interval.

Conclusions

The LCIA results reveal recycled cotton yarn is a viable alternative to relieve resource and environmental pressure. About 0.5 ha of agricultural land can be saved, 6600 kg CO₂ eq can be reduced, and 2783 m³ irrigation water can be saved by using 1000 kg of the recycled cotton yarns. It can be concluded that the recycled cotton fibers can be served as a substitute for virgin cotton fibers to reduce agricultural land and avoid environmental impacts generated from the cotton planting.

     

Gating of a G protein-sensitive mammalian Kir3.1 prokaryotic Kir channel chimera in planar lipid bilayers

Kir3 channels control heart rate and neuronal excitability through GTP-binding (G) protein and phosphoinositide signaling pathways. These channels were the first characterized effectors of the βγ subunits of G proteins. Because we currently lack structures of complexes between G proteins and Kir3 channels, their interactions leading to modulation of channel function are not well understood. The recent crystal structure of a chimera between the cytosolic domain of a mammalian Kir3.1 and the transmembrane region of a prokaryotic KirBac1.3 (Kir3.1 chimera) has provided invaluable structural insight. However, it was not known whether this chimera could form functional K(+) channels. Here, we achieved the functional reconstitution of purified Kir3.1 chimera in planar lipid bilayers. The chimera behaved like a bona fide Kir channel displaying an absolute requirement for PIP(2) and Mg(2+)-dependent inward rectification. The channel could also be blocked by external tertiapin Q. The three-dimensional reconstruction of the chimera by single particle electron microscopy revealed a structure consistent with the crystal structure. Channel activity could be stimulated by ethanol and activated G proteins. Remarkably, the presence of both activated Gα and Gβγ subunits was required for gating of the channel. These results confirm the Kir3.1 chimera as a valid structural and functional model of Kir3 channels.     

Clinorotation upregulates inducible nitric oxide synthase by inhibiting AP‐1 activation in human umbilical vein endothelial cells

Alterations of nitric oxide contribute to post‐flight orthostatic intolerance. The aim of this study was to investigate the changes of inducible nitric oxide synthase (iNOS) and the mechanisms underlying regulation of iNOS by simulated microgravity in human umbilical vein endothelial cells (HUVECs). Clinorotation, a simulated‐model of microgravity, increased iNOS expression and promoter activity in HUVECs. The transactivations of NF‐κB and AP‐1 were suppressed by 24 h clinorotation. A key role for AP‐1, but not NF‐κB in the regulation of iNOS was shown. (1) PDTC, a NF‐κB inhibitor, had no effect on clinorotation upregulation of iNOS. (2) SP600125, a JNK‐specific inhibitor, which resulted in inhibition of AP‐1 activity, enhanced the iNOS expression and promoter activity in clinorotation. (3) Overexpression of AP‐1 remarkably attenuated the upregulation effect of clinorotation. These findings indicate that clinorotation upregulates iNOS in HUVECs by a mechanism dependent on suppression of AP‐1, but not NF‐κB. These results support a key role for AP‐1 in the signaling of postflight orthostatic intolerance. J. Cell. Biochem. 107: 357–363, 2009. © 2009 Wiley‐Liss, Inc.     

The γ134.5 Protein of Herpes Simplex Virus 1 Is Required To Interfere with Dendritic Cell Maturation during Productive Infection

The γ₁34.5 protein of herpes simplex virus 1 is an essential factor for viral virulence. In infected cells, this viral protein prevents the translation arrest mediated by double-stranded RNA-dependent protein kinase R. Additionally, it associates with and inhibits TANK-binding kinase 1, an essential component of Toll-like receptor-dependent and -independent pathways that activate interferon regulatory factor 3 and cytokine expression. Here, we show that γ₁34.5 is required to block the maturation of conventional dendritic cells (DCs) that initiate adaptive immune responses. Unlike wild-type virus, the γ₁34.5 null mutant stimulates the expression of CD86, major histocompatibility complex class II (MHC-II), and cytokines such as alpha/beta interferon in immature DCs. Viral replication in DCs inversely correlates with interferon production. These phenotypes are also mirrored in a mouse ocular infection model. Further, DCs infected with the γ₁34.5 null mutant effectively activate naïve T cells whereas DCs infected with wild-type virus fail to do so. Type I interferon-neutralizing antibodies partially reverse virus-induced upregulation of CD86 and MHC-II, suggesting that γ₁34.5 acts through interferon-dependent and -independent mechanisms. These data indicate that γ₁34.5 is involved in the impairment of innate immunity by inhibiting both type I interferon production and DC maturation, leading to defective T-cell activation.Herpes simplex virus 1 (HSV-1) is a human pathogen responsible for localized mucocutaneous lesions and encephalitis (51). Following primary infection, HSV-1 establishes a latent or lytic infection in which the virus interacts with host cells, which include dendritic cells (DCs), required to initiate adaptive immune responses (36). Immature DCs, which reside in almost all peripheral tissues, are able to capture and process viral antigens (15). In this process, DCs migrate to lymph nodes, where they mature and present antigens to T cells. Mature DCs display high levels of major histocompatibility complex class II (MHC-II) and costimulatory molecules such as CD40, CD80, and CD86. Additionally, DCs release proinflammatory cytokines such as interleukin-12 (IL-12), tumor necrosis factor alpha, alpha interferon (IFN-α), and IFN-β, which promote DC maturation and activation. An important feature of functional DCs is to activate naïve T cells, and myeloid submucosal and lymph node resident DCs are responsible for HSV-specific T-cell activation (2, 45, 52). Moreover, DCs play a direct role in innate antiviral immunity by secreting type I IFN.HSV-1 is capable of infecting both immature and mature DCs (20, 24, 34, 38, 42). A previous study suggested that HSV entry into DCs requires viral receptors HVEM and nectin-2 (42). Upon HSV infection, plasmacytoid DCs detect viral genome through Toll-like receptor 9 (TLR9) and produce high levels of IFN-α (16, 23, 30, 40). In contrast, myeloid DCs, which are major antigen-presenting cells, recognize viral components through distinct pathways, independently of TLR9 (16, 36, 40). It has been suggested previously that HSV proteins or RNA intermediates produced during viral replication trigger myeloid DCs (16, 40). Indeed, a protein complex that consists of HSV glycoproteins B, D, H, and L stimulates the expression of CD40, CD83, CD86, and cytokines in myeloid DCs (41). Hence, DCs sense HSV through TLR-dependent and -independent mechanisms (16, 40, 41). Nevertheless, HSV replication compromises DC functions and subsequent T-cell activation (3, 20, 24, 42). HSV-1 interaction with immature DCs results in the downregulation of costimulatory molecules and cytokines (20, 34, 38, 42). While HSV-2 induces rapid apoptosis, HSV-1 does so with a delayed kinetics in human DCs (4, 20, 38). HSV-1 is also reported to interfere with functions of mature DCs (24, 39). Upon infection, HSV-1 induces the degradation of CD83 but not CD80 or CD86 in mature DCs (24, 25). Additionally, HSV-1 reduces levels of the chemokine receptors CCR7 and CXCR4 on mature DCs and subsequently impairs DC migration to the respective chemokine ligands CCL19 and CXCL12 (39).Although HSV infection impairs DC functions, viral components responsible for this impairment have not been thoroughly investigated. It has been suggested previously that the virion host shut-off protein (vhs) of HSV-1 contributes partially to the viral block of DC activation (43). This activity is thought to stem from the ability of vhs to destabilize host mRNA. Emerging evidence suggests that ICP0 perturbs the function of mature DCs, where it mediates CD83 degradation via cellular proteasomes (25). Findings from related studies show that ICP0 inhibits the induction of IFN-stimulated genes mediated by IFN regulatory factor 3 (IRF3) or IRF7 in other cell types (11, 27, 32, 33). However, the link of ICP0 activities to DC maturation remains to be established. Recently, we found that γ₁34.5, an HSV virulence factor, associates with and inhibits TANK-binding kinase 1 (TBK1), an essential component of TLR-dependent and -independent pathways that activates IRF3 and cytokine expression (49). Interestingly, an HSV mutant lacking γ₁34.5 stimulates MHC-II surface expression in glioblastoma cells (47). These observations raise the hypothesis that γ₁34.5 may modulate DC maturation during HSV infection.In this study, we report that γ₁34.5 is required to perturb DC maturation during HSV infection, leading to impaired T-cell activation. Wild-type virus, but not the γ₁34.5 null mutant, suppresses the expression of costimulatory molecules as well as cytokines in DCs. We provide evidence that the viral block of DC maturation is associated with reduced IFN-α/β secretion. Furthermore, the expression of γ₁34.5 inhibits DC-mediated allogeneic T-cell activation and IFN-γ production. IFN-neutralizing antibodies partially reverse DC maturation induced by the γ₁34.5 null mutant. These results shed light on the role of γ₁34.5 relevant to DC maturation and T-cell responses in HSV infection.     

Involvement of CD147 in overexpression of MMP-2 and MMP-9 and enhancement of invasive potential of PMA-differentiated THP-1

Background  

During infection and inflammation, circulating blood monocytes migrate from the intravascular compartments to the extravascular compartments, where they mature into tissue macrophages. The maturation process prepares the cells to actively participate in the inflammatory and immune responses, and many factors have been reported to be involved in the process. We found in our study that CD147 played a very important role in this process.     

Syntheses and 1D structures of organic-inorganic hydrid polymers combining M(ClO4)2 (M = Cd, Zn) junctions and the semi-flexible bis-pyridyl ligand 3-pmpmd (N,N′-bis(3-pyridylmethyl)pyromellitic diimide)

Two 1D organic-inorganic coordination polymers, [Cd(3-pmpmd)(CH₃CN)₂(H₂O)₂]_n · 2n(ClO₄)₂ (1) and [Zn(3-pmpmd)_1.5(H₂O)₂]_n · 2n(ClO₄)₂ · nCH₃CN (2), were obtained from M(ClO₄)₂ (M = Cd, Zn) and the semi-flexible 3,3′-N-donor bis-pyridyl ligand 3-pmpmd: 1 has an 1D zigzag framework with 3-pmpmd in the Z_T-mode (anti, trans-) conformation, while 2 has an 1D rod and loop network with 3-pmpmd in both Z_T- and Z_C-mode (anti, cis-) conformations. Results showed that the metal ions could influence the coordination mode of a semi-flexible bis-pyridyl ligand.