Periodontal inflammation is associated with an enhancement of both the M1 and M2 phenotypes of macrophages, in which a phenotypic switch of M2 to M1 might be a critical mechanism in mediating periodontal tissue damage, including alveolar bone loss.

The regimes of possible global atmospheric circulation patterns in an Earth‐like atmosphere are explored using a simplified Global Circulation Model (GCM) based on the University of Hamburg's Portable University Model for the Atmosphere (PUMA)—with simplified (linear) boundary‐layer friction, a Newtonian cooling scheme, and dry convective adjustment (designated here as PUMA‐S). A series of controlled experiments is conducted by varying planetary rotation rate and imposed equator‐to‐pole temperature difference. These defining parameters are combined further with each other into dimensionless forms to establish a parameter space in which the occurrences of different circulation regimes are mapped and classified. Clear, coherent trends are found when varying planetary rotation rate (thermal Rossby number) and frictional and thermal relaxation time‐scales. The sequence of circulation regimes as a function of parameters, such as the planetary rotation rate, strongly resembles that obtained in laboratory experiments on rotating, stratified flows, especially if a topographic β‐effect is included in those experiments to emulate the planetary vorticity gradients in an atmosphere induced by the spherical curvature of the planet. A regular baroclinic wave regime is also obtained at intermediate values of thermal Rossby number and its characteristics and dominant zonal wavenumber depend strongly on the strength of radiative and frictional damping. These regular waves exhibit some strong similarities to baroclinic storms observed on Mars under some conditions. Multiple jets are found at the highest rotation rates, when the Rossby deformation radius and other eddy‐related length‐scales are much smaller than the radius of the planet. These exhibit some similarity to the multiple zonal jets observed on gas giant planets. Jets form on a scale comparable to the most energetic eddies and the Rhines scale poleward of the supercritical latitude. The balance of heat transport varies strongly with Ω∗ between eddies and zonally symmetric flows, becoming weak with fast rotation.

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Obesity may paralyze innate immune response of periodontium via attenuating infiltration and activation of macrophages and further aggravate periodontal disease.

Background/Aims: The invasion of trophoblast cells into the maternal uterine decidua is critical for normal placentation, establishment of pregnancy and maintenance of fetal growth in humans. Several growth factors and cytokines have been implicated in trophoblast invasion, but the underlying regulatory mechanisms of invasion are not fully understood. Our earlier studies have found that caudal-related homeobox transcription factor 2 (CDX2) is hypomethylated in human pre-eclampsia placental tissues. However, whether CDX2 is involved in trophoblast invasion was unclear. Methods and Results: In this study, we investigated CDX2 function using a human HTR-8/SVneo cell line that overexpressed CDX2. Cell invasion assays demonstrated that CDX2 enhanced trophoblast cell invasiveness. Meanwhile, MTT assays revealed that CDX2 did not affect cell proliferation. Western blot analysis and quantitative real-time PCR demonstrated that the expression level of matrix metalloproteinase-9 (MMP-9) was significantly increased, whereas the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) was markedly suppressed in the CDX2-overexpressing trophoblast cells. The phosphoinositide-3-kinase (PI3K)/Akt signaling pathway is involved in proliferation, migration, metastasis and invasion. Our study showed that inhibition of PI3K/Akt signaling led to decreased expression of CDX2. Conclusion: We concluded that CDX2 is likely regulated by the PI3K/Akt signaling pathway during trophoblast cell invasion. Our findings may reveal new insights into the regulatory mechanisms of trophoblast cell invasion and may be an important contributor to the pathogenesis of pregnancy-related diseases.