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Geometry and kinematics have been intimately connected in their historical evolution and, although it is currently less fashionable, the further development of such connections is crucial to many computer-aided design and manufacturing. In this paper, the evolution of the translation surfaces and their generating curves in E3 are investigated. Integrability conditions of the Gauss-Weingarten equations are obtained. Kinematics of moving frame fields associated to these surfaces are described. The evolution equations of the Christoffel symbols, the second fundamental quantities and Gauss-Codazzi equations for the motion are established. Thus, the evolution equations of the curvatures in terms of their intrinsic geometric formulas are derived. Two examples of translation surfaces and their motions are considered and plotted.

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by abnormal autoreactivity in B cells. Lymphocytes and their soluble mediators contribute to the disease pathogenesis. We recently demonstrated that infecting lupus mice with malaria confers protection against lupus nephritis by attenuating oxidative stress in both liver and kidney tissues. In the current study, we further investigated B cell autoreactivity in female BWF1 lupus mice after infection with either live or gamma-irradiated malaria, using ELISA, flow cytometry and Western blot analysis. The lupus mice exhibited a significant elevation in plasma levels of IL-4, IL-6, IL-7, IL-12, IL-17, IFN-α, IFN-γ, TGF-β, BAFF and APRIL and a marked elevation of IgG2a, IgG3 and ant-dsDNA autoantibodies compared with normal healthy mice. Infecting lupus mice with live but not gamma-irradiated malaria parasite partially and significantly restored the levels of the soluble mediators that contribute to the progression of lupus. Furthermore, the B cells of lupus mice exhibited an increased proliferative capacity; aberrant overexpression of the chemokine receptor CXCR4; and a marked elevation in responsiveness to their cognate ligand (CXCL12) via aberrant activation of the PI3K/AKT, NFκB and ERK signaling pathways. Interestingly, infecting lupus mice with live but not gamma-irradiated malaria parasite restored a normal proliferative capacity, surface expression of CXCR4 and B cell response to CXCL-12. Taken together, our data present interesting findings that clarify, for the first time, the molecular mechanisms of how infection of lupus mice with malaria parasite controls B cell autoreactivity and thus confers protection against lupus severity.

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by abnormal autoreactivity in B cells. Lymphocytes and their soluble mediators contribute to the disease pathogenesis. We recently demonstrated that infecting lupus mice with malaria confers protection against lupus nephritis by attenuating oxidative stress in both liver and kidney tissues. In the current study, we further investigated B cell autoreactivity in female BWF1 lupus mice after infection with either live or gamma-irradiated malaria, using ELISA, flow cytometry and Western blot analysis. The lupus mice exhibited a significant elevation in plasma levels of IL-4, IL-6, IL-7, IL-12, IL-17, IFN-α, IFN-γ, TGF-β, BAFF and APRIL and a marked elevation of IgG2a, IgG3 and ant-dsDNA autoantibodies compared with normal healthy mice. Infecting lupus mice with live but not gamma-irradiated malaria parasite partially and significantly restored the levels of the soluble mediators that contribute to the progression of lupus. Furthermore, the B cells of lupus mice exhibited an increased proliferative capacity; aberrant overexpression of the chemokine receptor CXCR4; and a marked elevation in responsiveness to their cognate ligand (CXCL12) via aberrant activation of the PI3K/AKT, NFκB and ERK signaling pathways. Interestingly, infecting lupus mice with live but not gamma-irradiated malaria parasite restored a normal proliferative capacity, surface expression of CXCR4 and B cell response to CXCL-12. Taken together, our data present interesting findings that clarify, for the first time, the molecular mechanisms of how infection of lupus mice with malaria parasite controls B cell autoreactivity and thus confers protection against lupus severity.

Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by abnormal autoreactivity in B cells. Lymphocytes and their soluble mediators contribute to the disease pathogenesis. We recently demonstrated that infecting lupus mice with malaria confers protection against lupus nephritis by attenuating oxidative stress in both liver and kidney tissues. In the current study, we further investigated B cell autoreactivity in female BWF1 lupus mice after infection with either live or gamma-irradiated malaria, using ELISA, flow cytometry and Western blot analysis. The lupus mice exhibited a significant elevation in plasma levels of IL-4, IL-6, IL-7, IL-12, IL-17, IFN-α, IFN-γ, TGF-β, BAFF and APRIL and a marked elevation of IgG2a, IgG3 and ant-dsDNA autoantibodies compared with normal healthy mice. Infecting lupus mice with live but not gamma-irradiated malaria parasite partially and significantly restored the levels of the soluble mediators that contribute to the progression of lupus. Furthermore, the B cells of lupus mice exhibited an increased proliferative capacity; aberrant overexpression of the chemokine receptor CXCR4; and a marked elevation in responsiveness to their cognate ligand (CXCL12) via aberrant activation of the PI3K/AKT, NFκB and ERK signaling pathways. Interestingly, infecting lupus mice with live but not gamma-irradiated malaria parasite restored a normal proliferative capacity, surface expression of CXCR4 and B cell response to CXCL-12. Taken together, our data present interesting findings that clarify, for the first time, the molecular mechanisms of how infection of lupus mice with malaria parasite controls B cell autoreactivity and thus confers protection against lupus severity.

Bulk glasses and thin films of Ge20Se50Te30 were prepared by melt-quenching and thermal evaporation technique, respectively. The stoichiometry of the composition was checked by energy dispersive X-ray diffraction (EDX), whereas the crystallization was investigated using differential scanning calorimetery (DSC). The effect of heat treatment on the structure transformation of Ge20Se50Te30 films was determined by X-ray diffraction (XRD). The XRD results reveal that the as-prepared films are amorphous in nature while the annealed ones show crystalline phases. Further, the average crystallite size, strain, and dislocation density were found to depend on the annealing temperature. The optical transmittance and reflectance of the studied films at different annealing temperatures were measured using spectrophotometer. The optical parameters were calculated as a function of annealing temperature. The optical transition was found to be allowed indirect transition with optical band gap decreases from 1.69 to 1.41 eV with increasing the annealing temperature from 553 to 633 K.

Abstract
In insects, like in other animals, experience-based modulation of preference, a form of phenotypic plasticity, is common in heterogeneous environments. However, the role of multiple fitness-relevant experiences on insect preference remains largely unexplored. For the multivoltine polyphagous moth Spodoptera littoralis we investigated effects of larval and adult experiences on subsequent reproductive behaviours. We demonstrate, for the first time in male and female insects,that mating experience on a plant modulates plant preference in subsequent reproductive behaviours, whereas exposure to the plant alone or plant together with sex pheromone does not affect this preference. When including larval feeding experiences, we found that both larval rearing and adult mating experiences modulate host plant preference. These findings represent the first evidence that host plant preferences in polyphagous insects are determined by a combination of innate preferences modulated by sensory feedback triggered by multiple rewarding experiences throughout their lifetime.

Small interfering RNA (siRNA) is a powerful gene silencing tool and has been considered a potential agent for
the treatment of many diseases. However, development of safe and effective siRNA delivery systems still
remains a great challenge. In this study, we developed a new siRNA delivery system based on the
electrostatic encapsulation of siRNA/cationic vector complexes with dendrimer-like polymeric DNAs
(YY-DNAs). The binary complexes of siRNA with cationic vectors such as lipofectamine (LP),
polyethylenimine (PEI) and poly-L-lysine (PLL) were first constructed. Then, the encapsulation was
performed by the addition of YY-DNAs to the binary complexes in order to form stable complexes of
siRNA/LP/YY-DNAs, siRNA/PEI/YY-DNAs and siRNA/PLL/YY-DNAs. The encapsulated siRNA complexes
showed nearly spherical morphology with about 13–37 nm average hydrodynamic size and their
z-potentials were negative. The cationic complexes of siRNA/LP, siRNA/PEI and siRNA/PLL showed a
high cytotoxicity towards the cells and strong aggregation with erythrocytes, while their encapsulation
into YY-DNAs dramatically decreased the toxicities of complexes. Furthermore, these anionic
encapsulated siRNA complexes were highly taken up by the HeLa cells and showed extremely high
cellular uptake efficiencies and gene silencing effects without such cytotoxicity and aggregation. The
stability of these complexes in 10% FBS and human serum was investigated and they showed high
stability even after incubation for 72 h and 48 h, respectively. Therefore, we have newly identified safe
and efficient anionic complexes of siRNA for clinical uses.

Our present study provides an expedient general approach for the synthesis of some novel bridged dibenzo-azocinone,
-azoninone, -azecinone, -azocine, -azonine, and -azecine derivatives via Friedel–Crafts intramolecular ring-closure
reactions. The methodology is realized by a four-step protocol involving first preparation of 7-methyl-3,3-diphenylindoline
through the reduction of 7-methyl-3,3-diphenylindolin-2-one followed by N-alkylations with different haloesters (a-, b- or
g-). The resulting indoline ester derivatives were allowed to react both by addition of Grignard reagents to afford alcohols
and by hydrolysis to afford acids. Particular attention has been given to the novel structures especially in regard to the
promising pharmaceutical and therapeutic values associated with their skeletons.

Our present study provides an expedient general approach for the synthesis of some novel bridged dibenzo-azocinone,
-azoninone, -azecinone, -azocine, -azonine, and -azecine derivatives via Friedel–Crafts intramolecular ring-closure
reactions. The methodology is realized by a four-step protocol involving first preparation of 7-methyl-3,3-diphenylindoline
through the reduction of 7-methyl-3,3-diphenylindolin-2-one followed by N-alkylations with different haloesters (a-, b- or
g-). The resulting indoline ester derivatives were allowed to react both by addition of Grignard reagents to afford alcohols
and by hydrolysis to afford acids. Particular attention has been given to the novel structures especially in regard to the
promising pharmaceutical and therapeutic values associated with their skeletons.